Bleeding and Shock: Emergency Medical Care Essentials
1. Introduction: The Criticality of Bleeding and Shock
The provided sources emphasize a significant paradigm shift in emergency medical care: bleeding is now recognized as one of the most time-sensitive conditions paramedics face, superseding the previous primary focus on airway management. Any form of bleeding poses a potential danger, as it can ultimately lead to shock, a life-threatening state of cardiovascular system collapse resulting in inadequate tissue perfusion. Prompt treatment is paramount, as untreated shock can lead to vital organ damage and death.
2. Anatomy and Physiology of the Cardiovascular System
The cardiovascular system's crucial function is to maintain blood flow, which serves to deliver oxygen and nutrients to peripheral tissues while removing gaseous waste products (carbon dioxide) and other metabolic wastes.
Key Components:
• Heart: A muscular, cone-shaped organ (avg. 280-350g in men, 225-280g in women) located behind the sternum, responsible for pumping blood. It has four chambers: two atria (receiving blood) and two ventricles (pumping blood out).
◦ Blood Flow: Deoxygenated blood enters the right atrium (via vena cava), passes to the right ventricle, then to the lungs (via pulmonary artery). Oxygenated blood returns to the left atrium (via pulmonary veins), flows to the left ventricle, and is then pumped into the aorta for systemic circulation.
• Blood: Composed of plasma (92% water, 8% dissolved substances) and formed elements:
◦ Red Blood Cells (Erythrocytes): Most numerous, disc-shaped, contain hemoglobin for oxygen transport.
◦ White Blood Cells (Leukocytes): Fight infection.
◦ Platelets: Small cells essential for clot formation (hemostasis) to control bleeding.
• Blood Vessels: Arteries, veins, arterioles, capillaries, and venules form the network for blood circulation.
Perfusion:
• Definition: The circulation of blood within an organ or tissue in adequate amounts to meet the cells' current needs for oxygen, nutrients, and waste removal.
• Critical Balance: Blood must flow fast enough for adequate circulation, but slow enough for cellular exchange of oxygen, nutrients, and waste products.
• Organ Tolerance to Hypoperfusion (at 37.0°C):
◦ Heart: Requires constant perfusion.
◦ Brain and Spinal Cord: Cannot go more than 4-6 minutes.
◦ Kidneys: Permanently damaged after 45 minutes.
◦ Skeletal Muscles: Tolerate up to 2 hours.
◦ GI Tract: Can exist with limited perfusion for several hours.
◦ Note: Colder temperatures increase resistance to damage due to slowed metabolism.
Cardiac Cycle and Output:
• Cardiac Output: The amount of blood pumped through the circulatory system in 1 minute (L/min), calculated as pulse rate multiplied by stroke volume.
• Starling Law of the Heart: Increased venous return stretches ventricles, resulting in increased cardiac contractility to maintain normal cardiac function.
3. Pathophysiology and Significance of Hemorrhage
Hemorrhage simply means bleeding, ranging from minor to life-threatening.
Types of Hemorrhage:
• External Bleeding: Visible blood loss due to a break in the skin.
◦ Capillary bleeding: Oozes.
◦ Venous bleeding: Flows steadily, darker red.
◦ Arterial bleeding: Spurts in time with the pulse, bright red, difficult to control.
• Internal Bleeding: Occurs within the body, often from trauma (e.g., ruptured spleen, long bone/pelvic fractures, major vascular injuries) or nontraumatic causes (e.g., GI bleeding, ruptured ectopic pregnancies, ruptured aneurysms).
◦ Signs may not develop quickly, requiring reliance on other symptoms like pain, tenderness, tachycardia, pallor, and the development of shock.
Significance of Blood Loss:
• Total Blood Volume: Adult males: approx. 70 mL/kg; adult females: approx. 65 mL/kg.
• Tolerance: The body cannot tolerate an acute loss of more than 20% of total blood volume.
• Impact: Losing more than 1 liter of blood in a typical adult (or smaller amounts in children/infants) causes significant changes in vital signs (increased heart/respiratory rates, decreasing blood pressure). Rapid blood loss can quickly lead to hypovolemic shock.
• Serious Bleeding Indicators: Significant mechanism of injury (MOI), poor patient appearance, signs/symptoms of shock, significant blood loss, hemodynamic instability, or uncontrollable bleeding.
Physiologic Response to Hemorrhage:
• Natural Clotting (Hemostasis): Bleeding tends to stop within about 10 minutes due to vessel narrowing and platelet aggregation at the injury site, forming a clot. Clotting factors are triggered by contact with body tissues, fluids, or the external environment.
• Failure of Hemostasis: Can occur due to medications, severe injury, or if only part of the vessel wall is cut. Acute blood loss may result in death before natural clotting mechanisms can help.
• Trauma Triad of Death: A critical combination of hypothermia, coagulopathy (poor blood clotting), and acidosis that significantly increases mortality in trauma patients. Management focuses on aggressively controlling bleeding, keeping patients warm, and minimizing acidic IV fluids.
4. Understanding Shock: The State of Hypoperfusion
Shock is defined as a "state of collapse and failure of the cardiovascular system that causes inadequate tissue perfusion." It is not a specific disease but rather a complex physiological response to inadequate blood flow to the body's cells, leading to a failure to rid the body of metabolic wastes. Hypoperfusion is the underlying issue, where tissue perfusion decreases below normal, leading to cellular ischemia and a switch from aerobic to less efficient anaerobic metabolism.
Mechanisms of Shock:
Normal tissue perfusion requires an intact heart, blood/body fluids, and blood vessels. Damage to any of these can lead to shock.
• Cardiogenic Shock: Failure of the heart's pumping ability (e.g., myocardial infarction, arrhythmias, severe acidosis). Leads to insufficient blood circulation and inadequate oxygen delivery.
• Hypovolemic Shock: Loss of fluid volume.
◦ Hemorrhagic Shock: Most common cause, specifically from blood loss (external or internal).
◦ Other fluid loss: Plasma, electrolyte solution (e.g., dehydration, burns, crush injury, anaphylaxis).
• Neurogenic Shock: Failure of vasoconstriction, usually from spinal cord injury, leading to loss of sympathetic nervous system tone and widespread vasodilation below the injury level. This causes blood to pool in expanded vascular beds, resulting in relative hypovolemia and inadequate perfusion. Characterized by warm, pink, dry skin and absence of sweating below the injury level.
• Distributive Shock: Widespread dilation of blood vessels, causing circulating blood volume to pool and tissue perfusion to decrease. Types include:
◦ Septic Shock: Result of widespread infection leading to an uncontrolled inflammatory-immune response, causing hypoperfusion, tissue destruction, and organ death.
◦ Anaphylactic Shock: Severe allergic reaction causing widespread vascular dilation, relative hypovolemia, bronchoconstriction, and fluid leakage into interstitial spaces.
Compensation for Decreased Perfusion:
The body employs compensatory mechanisms to maintain blood pressure and perfusion:
• Baroreceptors: Detect drops in arterial pressure, stimulating the sympathetic nervous system and vasoconstrictor center of the medulla.
• Hormonal Release: Renin-angiotensin-aldosterone system and antidiuretic hormone (ADH) are activated, triggering salt and water retention and peripheral vasoconstriction.
• Adrenal Gland Hormones: Epinephrine and norepinephrine are released, increasing pulse rate, strength of contraction, and peripheral vascular resistance (vasoconstriction).
• Spleen: Releases sequestered red blood cells. These mechanisms aim to increase preload, stroke volume, and pulse rate, thereby increasing cardiac output. However, if hypoperfusion persists, these mechanisms fail, leading to progressive deterioration.
Phases of Shock:
1. Compensated Shock (Earliest Stage): The body can still compensate for blood loss (up to 15-30% in hemorrhagic shock). Blood pressure is maintained. Level of responsiveness is the best indicator of tissue perfusion. Treatment at this stage usually leads to recovery.
2. Decompensated Shock: Blood pressure is falling (a late sign). Blood volume drops by more than 30%. Compensatory measures begin to fail, and signs/symptoms become more obvious. Cardiac output falls dramatically. Treatment sometimes results in recovery.
3. Irreversible Shock: The final, fatal stage where accumulating acids and waste products act as vasodilators, further decreasing venous return and diminishing blood flow. Organ failure becomes evident, ultimately leading to multiple-organ dysfunction syndrome (MODS) and death.
Systemic Inflammatory Response Syndrome (SIRS):
A systemic inflammatory response to severe clinical insults, not always indicative of infection. SIRS + infection = sepsis. Manifested by two or more of:
• Temperature >38°C or <36°C
• Heart rate >90 beats/min
• Respiratory rate >20 breaths/min or PCO2 <32 mm Hg
• White blood cell count >12 × 10^9 cells/L or <4 × 10^9 cells/L Uncontrolled SIRS can lead to hypotension, inadequate perfusion, and ultimately MODS and death.
5. Assessment and Management in the Field
Immediate action and rapid transport are crucial in managing bleeding and shock.
General Assessment:
• Scene Assessment: Evaluate hazards and the mechanism of injury (MOI) to predict potential internal injuries or bleeding. Always use appropriate personal protective equipment (PPE: gloves, mask, eyeshield, gown).
• Initial Assessment: Determine mental status. Immediately manage life threats to airway, breathing, and circulation. Control major external bleeding immediately. Suspected internal bleeding requires warmth and supplemental oxygen, with rapid transport as the priority.
• Prioritization: Patients in shock are high priority. Time is of the essence; on-scene care should be limited to essential items, and extensive history taking (SAMPLE) and baseline vital signs can be performed en route to the hospital. "Delay inserting IV lines until en route."
Management of External Hemorrhage:
1. Direct Pressure: Apply direct pressure over the wound.
2. Elevation: Elevate the injured area above heart level if no fracture is suspected.
3. Pressure Dressing: Apply a pressure dressing.
4. Tourniquet: Generally a last resort for severe external bleeding on an extremity that cannot be controlled by other means or for amputations. Apply widest bandage possible, never over a joint, use wide padding, never cover with a bandage, and do not loosen after application.
5. Wound Packing: Effective for deep, gaping wounds, especially in junctional areas (e.g., groin), to contact the source of bleeding and fill the cavity.
Special Management Techniques:
• Fractures: Immobilize unstable fractures (using air splints, rigid splints, or traction splints) to control bleeding from lacerated vessels and tissues caused by bone movement.
• Hemostatic Agents: Enhance clot formation at the wound site.
• Pelvic Binder: Applied for suspected pelvic fractures (pain, signs of hypovolemic shock, suspicious MOI) to reduce the fracture, provide mechanical stability, and control massive bleeding.
Managing Internal Hemorrhage:
• Definitive Treatment: Occurs in the hospital (surgical procedure).
• Prehospital Management: Primarily focuses on treating for shock and rapid transport.
◦ Keep the patient supine and warm.
◦ Maintain an open airway, check breathing and pulse.
◦ Administer high-flow supplemental oxygen; assist ventilation if needed.
◦ Splint broken bones or joint injuries; apply pelvic binder if indicated.
◦ Insert a large-bore IV catheter en route (unless transport is delayed) and administer a fluid challenge of 250 mL crystalloid if hypoperfusion is present. Use warm IV fluids.
◦ Consider pain medication.
◦ Monitor serial vital signs.
IV Fluid Therapy:
• Purpose: Immediate fluid replacement or potential fluid replacement.
• Fluids of Choice: Normal saline or lactated Ringer solution. Dextrose in water solutions are ineffective for volume restoration.
• Permissive Hypotension: For hemorrhagic shock, evidence suggests titrating systolic blood pressure to 80-90 mm Hg may allow for better clotting and prevent dislodging formed clots. This approach needs careful consideration of the entire patient.
• Volume Expanders: Indicated for hypovolemic, obstructive, and spinal shock to replace lost volume or "fill the container" in relative hypovolemia.
Transportation:
• Urgency: "Transport is inevitable." The key questions are when and where.
• Destination: Patients with severe internal/external bleeding or cardiogenic shock are time-sensitive and should be transported rapidly to a regional trauma center or facility with surgical capabilities, potentially via helicopter.
• Communication: "Calling ahead" to notify the emergency department (ED) is vital for patient readiness and improved outcomes.
6. Case Study Application and Key Takeaways
The case study of the gunshot victim highlights critical principles:
• Hidden Bleeding: "Does the lack of significant visible bleeding and the fact that he is alert indicate that this patient is not bleeding seriously?" No. Internal bleeding can be severe without overt external signs. The inability to palpate a radial pulse indicates severe hypoperfusion.
• Time Sensitivity: "What is the significance of time in this type of incident?" Time is paramount. The "golden hour of trauma" emphasizes the critical window for intervention. Organ viability is severely limited by sustained hypoperfusion (e.g., brain and spinal cord for 4-6 minutes, kidneys for 45 minutes).
• Blood Volume Calculation: For an 80 kg adult male, the total blood volume is approximately 80 kg * 70 mL/kg = 5600 mL (5.6 liters). An acute loss of more than 20% (1.12 liters) is poorly tolerated and leads to significant vital sign changes.
• Shock Phase: The patient's confusion, nausea, thirst, and absent radial pulse (despite being alert initially) strongly suggest he is in the decompensated phase of shock, where compensatory mechanisms are failing, and blood pressure is dropping.
• Interventions:
◦ BLS: Immediate direct pressure to the wound, maintaining supine position, high-flow supplemental oxygen, keeping the patient warm. Rapid transport is a critical BLS intervention.
◦ ALS: Early large-bore IV access and fluid challenges (normal saline) en route to the hospital, continuous monitoring of vital signs (mental status, pulse, BP, SpO2), and preparation for ventilatory assistance if mental status deteriorates further. Spinal immobilization was correctly deferred given the patient's reported lack of being "blown to the ground" and the need for rapid transport due to hemorrhagic shock.
• Benefit of Rapid Transport and Communication: The case demonstrates that prompt judgment to save on-scene time and early communication with the ED can significantly reduce time to definitive surgical intervention, which "was the patient's best chance," leading to improved survival.
In conclusion, effective management of bleeding and shock requires rapid recognition, aggressive hemorrhage control, treatment for hypoperfusion, maintaining body temperature, and swift transport to a facility capable of definitive care. The focus has shifted to controlling bleeding as the primary and most time-sensitive intervention, recognizing the critical role of timely surgical intervention for severe internal hemorrhage.